Pain
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Randomized Controlled Trial
The association of acetazolamide infusion with headache and cranial artery dilation in healthy volunteers.
The carbonic anhydrase inhibitor acetazolamide causes extracellular acidosis and dilatation of cerebral arterioles. In this study, we tested the hypothesis that acetazolamide also may induce headache and dilatation of cranial arteries. In a randomized double-blind crossover study design, 12 young healthy women were allocated to injection of 1 g acetazolamide or placebo on 2 separate days. ⋯ Compared to placebo, arterial circumference increased after acetazolamide in the basilar artery (P=.002) as well as the cerebral (P=.003), cavernous (P=.002), and cervical (P=.005) parts of the internal carotid artery, but no other extracranial arteries changed after acetazolamide. In conclusion, acetazolamide caused immediate and delayed headache as well as dilatation of intracranial arteries in healthy volunteers. It is possible that extracellular acidosis induced by acetazolamide causes sensitization of cephalic perivascular nociceptors, which, in combination with vasodilatation, leads to delayed headache.
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Fibromyalgia typically presents with spontaneous body pain with no apparent cause and is considered pathophysiologically to be a functional disorder of somatosensory processing. We have investigated potential associations between the degree of self-reported clinical pain and resting-state brain functional connectivity at different levels of putative somatosensory integration. Resting-state functional magnetic resonance imaging was obtained in 40 women with fibromyalgia and 36 control subjects. ⋯ The results confirm previous research demonstrating abnormal functional connectivity in fibromyalgia and show that alterations at different levels of sensory processing may contribute to account for clinical pain. Importantly, reduced functional connectivity extended beyond the somatosensory domain and implicated visual and auditory sensory modalities. Overall, this study suggests that a general weakening of sensory integration underlies clinical pain in fibromyalgia.
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Randomized Controlled Trial
Short-term Improvement in Insomnia Symptoms Predicts Long-term Improvements in Sleep, Pain, and Fatigue in Older Adults with Co-Morbid Osteoarthritis and Insomnia.
In a primary care population of 367 older adults (aged ⩾60 years) with osteoarthritis (OA) pain and insomnia, we examined the relationship between short-term improvement in sleep and long-term sleep, pain, and fatigue outcomes through secondary analyses of randomized controlled trial data. Study participants, regardless of experimental treatment received, were classified either as improvers (⩾30% baseline to 2-month reduction on the Insomnia Severity Index [ISI]) or as nonimprovers. After controlling for treatment arm and potential confounders, improvers showed significant, sustained improvements across 18 months compared with nonimprovers in pain severity (P<0.001, adjusted mean difference=-0.51 [95% CI: -0.80, -0.21), arthritis symptoms (P<0.001, 0.63 [0.26, 1.00]), and fear avoidance (P=0.009, -2.27 [-3.95, -0.58]) but not in catastrophizing or depression. Improvers also showed significant, sustained improvements in ISI (P<0.001, -3.03 [-3.74, -2.32]), Pittsburgh Sleep Quality Index Total (P<0.001, -1.45 [-1.97, -0.93]) and general sleep quality (P<0.001, -0.28 [-0.39, -0.16]) scores, Flinders Fatigue Scale (P<0.001, -1.99 [-3.01, -0.98]), and Dysfunctional Beliefs About Sleep Scale (P=0.037, -2.44 [-4.74, -0.15]), but no improvements on the Functional Outcomes of Sleep Questionnaire or the Epworth Sleepiness Scale. We conclude that short-term (2-month) improvements in sleep predicted long-term (9- and 18-month) improvements for multiple measures of sleep, chronic pain, and fatigue. These improvements were not attributable to nonspecific benefits for psychological well-being, such as reduced depression. These findings are consistent with benefits of improved sleep for chronic pain and fatigue among older persons with osteoarthritis pain and comorbid insomnia if robust improvements in sleep are achieved and sustained.
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Recent human neuroimaging studies have investigated the neural correlates of either noxious stimulus intensity or reported pain. Although useful, analyzing brain relationships with stimulus intensity and behavior separately does not address how sensation and pain are linked in the central nervous system. In this study, we used multi-level mediation analysis to identify brain mediators of pain--regions in which trial-by-trial responses to heat explained variability in the relationship between noxious stimulus intensity (across 4 levels) and pain. ⋯ Finally, several regions did not respond to noxious input, but their activity predicted pain; these included ventromedial prefrontal cortex, dorsolateral prefrontal cortex, cerebellar regions, and supplementary motor cortices. These regions likely underlie both nociceptive and non-nociceptive processes that contribute to pain, such as attention and decision-making processes. Overall, these results elucidate how multiple distinct brain systems jointly contribute to the central generation of pain.
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Randomized Controlled Trial
The emotion regulatory function of parent attention to child pain and associated implications for parental pain control behaviour.
We investigated the function of parental attention to child pain in regulating parental distress and pain control behaviour when observing their child performing a painful (cold pressor) task (CPT); we also studied the moderating role of parental state anxiety. Participants were 62 schoolchildren and one of their parents. Parental attention towards or away from child pain (ie, attend to pain vs avoid pain) was experimentally manipulated during a viewing task pairing unfamiliar children's neutral and pain faces. ⋯ Specifically, whereas low anxious parents reported more distress and demonstrated more pain control behaviour in the Attend to Pain condition, high anxious parents reported more distress and showed more pain control behaviour in the Avoid Pain condition. This inverse pattern was likewise apparent in physiological distress indices (HR) in response to the initial viewing task. Theoretical/clinical implications and further research directions are discussed.